OBJECTIVES: Biofilm formation is critical to dental caries initiation and development. The aim of this study was to investigate the effects of nicotine exposure on Streptococcus mutans (S. mutans) biofilm formation concomitantly with the inhibitory effects of sodium chloride (NaCl), potassium chloride (KCl) and potassium iodide (KI) salts. This study examined bacterial growth with varying concentrations of NaCl, KCl, and KI salts and nicotine levels consistent with primary levels of nicotine exposure. MATERIALS AND METHODS: A preliminary screening experiment was performed to investigate the appropriate concentrations of NaCl, KCl, and KI to use with nicotine. With the data, a S. mutans biofilm growth assay was conducted using nicotine (0–32 mg/mL) in Tryptic Soy broth supplemented with 1% sucrose with and without 0.45 M of NaCl, 0.23 M of KCl, and 0.113 M of KI. The biofilm was stained with crystal violet dye and the absorbance measured to determine biofilm formation. RESULTS: The presence of 0.45 M of NaCl, 0.23 M of KCl, and 0.113 M of KI significantly inhibited (p < 0.05) nicotine-induced S. mutans biofilm formation by 52%, 79.7%, and 64.1%, respectively. CONCLUSIONS: The results provide additional evidence regarding the biofilm-enhancing effects of nicotine and demonstrate the inhibitory influence of these salts in reducing the nicotine-induced biofilm formation. A short-term exposure to these salts may inhibit S. mutans biofilm formation.
Biofilms ; Dental Caries ; Gentian Violet ; Mass Screening ; Nicotine ; Potassium Chloride ; Potassium Iodide ; Salts ; Sodium Chloride ; Streptococcus mutans ; Streptococcus ; Sucrose

The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further utilization of post-surgical radioactive iodine (RAI) therapy, which is an effective treatment for reducing the risk of recurrence, and even the mortality, of DTC. Whereas, the dedifferentiation of DTC could influence the expression of functional NIS, thereby reducing the efficacy of RAI therapy in advanced DTC. Genetic alternations (such as BRAF and the rearranged during transfection [RET]/papillary thyroid cancer [PTC] rearrangement) have been widely reported to be prominently responsible for the onset, progression, and dedifferentiation of PTC, mainly through activating the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signaling cascades. These genetic alternations have been suggested to associate with the reduced expression of iodide-handling genes in thyroid cancer, especially the NIS gene, disabling iodine uptake and causing resistance to RAI therapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of these iodine-metabolizing genes and enhance iodine uptake through in vitro studies and studies of RAI-refractory (RAIR)-DTC patients. In this review, we discuss the regulation of NIS, known mechanisms of dedifferentiation including the MAPK and PI3K pathways, and the current status of redifferentiation therapy for RAIR-DTC patients.
Humans ; In Vitro Techniques ; Iodine ; Ion Transport ; Isotopes ; Mortality ; Protein Kinases ; Recurrence ; Sodium Iodide ; Thyroid Gland ; Thyroid Neoplasms ; Transfection

Radioiodine (RAI) has been used for the treatment of hyperthyroidism and is usually administered orally as sodium iodide (I-131) in solution or a capsule. However, this results in RAI being rapidly incorporated into the thyroid cells, and extensive local tissue damage occurring via beta emissions of I-131. The incidence rate of hypothyroidism is 5–50% at the first year after RAI therapy and is positively associated with the dosage of RAI. RAI has been used since 1960 in Korea; however, there have been few well-designed prospective trials, leaving many questions about indications, optimal dose, efficacy, and side-effects. This review summarizes the latest research pertaining to clinical questions about indications, optimal dose, efficacy, and side-effects.
Graves Disease ; Hyperthyroidism ; Hypothyroidism ; Incidence ; Korea ; Prospective Studies ; Sodium Iodide ; Thyroid Gland

Although radioiodine has been applied in thyroid diseases including carcinoma for over 70 years, it was only in 1996 that the basic molecular mechanism of iodine uptake was identified. Iodide is actively transported into the thyroid via a membrane glycoprotein known as sodium iodide symporter (NIS). NIS mediates radioiodine uptake into thyroid normal and cancer cells. The knowledge on NIS expression has provided scientific background to the empirical management of thyroid carcinoma. Based on recent studies of the NIS gene, this paper provides current clinical applications and future studies.
Genetic Therapy ; Humans ; Iodine ; Ion Transport ; Membrane Glycoproteins ; Sodium Iodide ; Sodium ; Theranostic Nanomedicine ; Thyroid Diseases ; Thyroid Gland ; Thyroid Neoplasms

Renal metastasis of thyroid cancer is extremely rare. We report the case of a 62-year-old woman with Hürthle cell thyroid cancer (HCTC) with lungs, bones, and bilateral kidneys metastases. The renal metastatic lesions were clearly demonstrated by ¹³¹I whole body scan (WBS) with SPECT/CT. However, they exhibited false-negative results in ¹⁸F-FDG PET/CT, kidney ultrasonography, and contrast-enhanced CT scan. The findings imply that tumors have low glucose metabolism and are able to accumulate radioiodine, which is not commonly found in the relatively aggressive nature of HCTC. The patient received two sessions of 200 mCi ¹³¹I therapy within 6 months duration. There was complete treatment response as evaluated by the second post-therapeutic ¹³¹I SPECT/CT and serum thyroglobulin. To our knowledge, renal metastasis from HCTC with positive ¹³¹I but negative ¹⁸F-FDGuptake has not been reported in the literature. This case suggests that ¹³¹I SPECT/CTis useful for lesion localization and prediction of ¹³¹I therapy response.
Female ; Glucose ; Humans ; Kidney ; Lung ; Metabolism ; Middle Aged ; Neoplasm Metastasis ; Positron-Emission Tomography and Computed Tomography ; Sodium Iodide ; Sodium ; Thyroglobulin ; Thyroid Gland ; Thyroid Neoplasms ; Tomography, X-Ray Computed ; Ultrasonography ; Whole Body Imaging

For the distant metastasis of differentiated thyroid cancers, such as papillary thyroid carcinoma, follicular thyroid carcinoma, and Hurthle cell carcinoma, radioiodine therapy is one of the standard treatment methods after total thyroidectomy. Radioiodine is accumulated in thyroid cells and thyroid cancer cells through sodium iodide symporter which is located in the membrane of cells. This molecular target specific therapy renders a better prognosis and less adverse effects. Radioiodine 131I emits gamma ray for imaging and beta ray for treatment at the same time, we can monitor patients' specific distribution of radioiodine, which let us know unexpected metastasis lesions or differentiated status of thyroid cancer cells. In this article, I reviewed practical points of view about radioiodine therapy for distant metastasis of thyroid cancers such as methods for administration of radioiodine, patients' preparation before radioiodine treatment, follow up of patients, adverse effects, and radiation safety issues.
Adenocarcinoma, Follicular ; Beta Particles ; Carcinoma ; Enzyme Multiplied Immunoassay Technique ; Follow-Up Studies ; Gamma Rays ; Humans ; Ion Transport ; Linear Energy Transfer ; Membranes ; Neoplasm Metastasis ; Organothiophosphorus Compounds ; Prognosis ; Sodium Iodide ; Symporters ; Thyroid Gland ; Thyroid Neoplasms ; Thyroidectomy

Iododerma is a rare cutaneous eruption that occurs after oral, parenteral or topical administration of iodides. Acneiform papulopustular lesions are the most common skin reactions of iododerma and erythematous, vesiculobullous, vegetative, and pustular psoriasis-like lesions appear less commonly. A 40-year-old woman with post-thyroidectomy presented with pustular and crusted patches with erythematous and indurated bases on the face and well-defined purplish crusted desquamative plaques on the lower legs at 10 days after radioactive iodine-131 ablation. Based on clinicopathological findings and history, she was diagnosed with iododerma following radioactive iodine ablation. Hypersensitivity to iodine is more uncommon in iodine-131 therapy compared with other iodine-containing substances since the quantity of sodium iodide is infinitely small. As iododerma following radioactive iodine ablation is a rare entity, so clinicians need to know about the possibilities of developing the skin lesion along with other early side effects before administering iodine-131 therapy.
Administration, Topical ; Female ; Humans ; Hypersensitivity ; Iodides ; Iodine ; Leg ; Skin ; Sodium Iodide ; Thyroid Gland ; Thyroid Neoplasms

BACKGROUND/AIMS: This study was performed to investigate the correlation of sodium iodide symporter (NIS) expression with the functionality and loss of phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression in human cholangiocarcinoma (CCA). METHODS: Immunohistochemistry for the expression of NIS and PTEN was performed in 60 biopsy specimens of CCA. The clinicopathological parameters were retrospectively identified from medical records. The expression pattern of NIS and loss of PTEN expression were analyzed in association with the clinicopathological characteristics, including survival. RESULTS: Normal biliary trees displayed NIS expression, but hepatocytes did not. NIS expression was divided into two patterns: cytoplasmic and membranous. Fifty-nine cases, all except for one case, displayed NIS expression in tumor cells. Twenty-two cases (33.3%) were mixed pattern, and 39 cases (65.05%) were cytoplasmic pattern; the pure membranous pattern was not noted. There was no association between the NIS expression pattern and clinicopathological parameters, including age, sex, differentiation grade, T stage and tumor, node, metastasis stage (p>0.05). The survival rates were similar among various NIS expression patterns. Normal hepatocytes and biliary trees exhibited PTEN expression in the nucleus and cytoplasm. CCA cells displayed nuclear staining. Thirty-six (60.0%) of 60 cases displayed a loss of PTEN expression. The loss of PTEN expression was observed in the advanced T-stage group (p=0.0036), but there was no association between the loss of PTEN expression and other clinicopathological parameters (p>0.05). No association between the loss of PTEN expression and survival was noted. CONCLUSIONS: NIS is expressed in most types of human CCA. The expression pattern suggests a role in cancer development. PTEN loss expression is common in the context of human CCA, especially in the advanced T stage.
Biopsy ; Cholangiocarcinoma ; Cytoplasm ; Hepatocytes ; Humans ; Immunohistochemistry ; Ion Transport ; Medical Records ; Microfilament Proteins ; Neoplasm Metastasis ; Retrospective Studies ; Sodium ; Sodium Iodide ; Survival Rate ; Symporters

Sunitinib malate is a multi-targeted tyrosine kinase inhibitor used for gastrointestinal stromal tumor and renal cell carcinoma. It is also under phase II trial for use in advanced colon cancer, non-small cell lung cancer and breast cancer. Sunitinib-induced thyroid dysfunction, mainly hypothyroidism is very common and is reported around 50~85% of sunitinib treated patients. The proposed mechanisms of sunitinib-induced hypothyroidism are 1) inhibition of thyroid peroxidase, 2) inhibition of sodium iodide symporter, and 3) destructive thyroiditis due to reduced vasculature through inhibition of VEGFR by sunitinib. Although nearly one third of patients with sunitinib-induced hypothyroidism would benefit from thyroid hormone replacement therapy, one should be cautious about use of thyroxine replacement therapy because hypothyroidism itself is associated with good prognosis in patients with various kinds of advanced cancer. Because of high prevalence of thyroid dysfunction observed with sunitinib, it is recommended to evaluate thyroid function before starting and during the use of sunitinib and thyroid hormone replacement should be considered both on the basis of patient's symptom and laboratory value. Future prospective studies to address the issue of prevalence, mechanism and treatment of sunitinib-induced hypothyroidism and its association with prognosis of advanced cancer is expected.
Breast Neoplasms ; Carcinoma, Non-Small-Cell Lung ; Carcinoma, Renal Cell ; Colonic Neoplasms ; Gastrointestinal Stromal Tumors ; Hormone Replacement Therapy ; Humans ; Hypothyroidism ; Indoles ; Iodide Peroxidase ; Ion Transport ; Prevalence ; Prognosis ; Protein-Tyrosine Kinases ; Pyrroles ; Sodium Iodide ; Symporters ; Thyroid Gland ; Thyroiditis ; Thyroxine

The present study was attempted to investigate whether polyphenolic compounds isolated from wine, which is brewed from Rubus coreanum Miquel (PCRC), may affect the release of catecholamines (CA) from the isolated perfused adrenal medulla of the spontaneously hypertensive rats (SHRs), and to establish its mechanism of action. PCRC (20~180 microgram/ml) perfused into an adrenal vein for 90 min relatively dose-dependently inhibited the CA secretory responses to ACh (5.32 mM), high K+ (56 mM), DMPP (100 micrometer) and McN-A-343 (100 micrometer). PCRC itself did not affect basal CA secretion (data not shown). Also, in the presence of PCRC (60 microgram/ml), the CA secretory responses to veratridine (a selective Na+ channel activator (10 micrometer), Bay-K-8644 (a L-type dihydropyridine Ca2+ channel activator, 10 micrometer), and cyclopiazonic acid (a cytoplasmic Ca2+ -ATPase inhibitor, 10 micrometer) were significantly reduced, respectively. In the simultaneous presence of PCRC (60 microgram/ml) and L-NAME (an inhibitor of NO synthase, 30 micrometer), the inhibitory responses of PCRC on the CA secretion evoked by ACh, high K+, DMPP, and Bay-K-8644 were considerably recovered to the extent of the corresponding control secretion compared with that of PCRC-treatment alone. The level of NO released from adrenal medulla after the treatment of PCRC (60 microgram/ml) was greatly elevated compared with the corresponding basal level. Taken together, these results demonstrate that PCRC inhibits the CA secretion from the isolated perfused adrenal medulla of the SHRs evoked by stimulation of cholinergic receptors as well as by direct membrane-depolarization. It seems that this inhibitory effect of PCRC is mediated by blocking the influx of calcium and sodium into the adrenal medullary chromaffin cells of the SHRs as well as by inhibition of Ca2+ release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of NO synthase.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Adrenal Medulla ; Calcium ; Catecholamines ; Chromaffin Cells ; Cytoplasm ; Dihydropyridines ; Dimethylphenylpiperazinium Iodide ; Indoles ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitric Oxide Synthase ; Polyphenols ; Rats, Inbred SHR ; Receptors, Cholinergic ; Sodium ; Veins ; Veratridine ; Wine